Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nucleot(s)ide analogues are making milestones in the treatment of chronic hepatitis B (CHB) as safe oral therapy. FDA approved lamivudine in adult patients in 1998, adefovir dipivoxil in 2002, and entecavir in March 2005. Lamivudine is effective in viral suppression, ALT normalization, and improvement in histology in both HBeAg positive and HBeAg negative / HBV DNA positive patients. HBeAg seroconversion rates correlate directly with pretreatment ALT levels at 18-30% after one year of therapy. Hepatitis flares may occur if lamivudine is stopped before HBeAg seroconversion. Lamivudine resistant YMDD mutants emerge at a rate of 15-20% per year of therapy; often associated with the rebound viraemia, relapse of hepatitis or even hepatic decompensation. Durability of response off lamivudine therapy is not satisfactory and may be dependent on duration of therapy post-seroconversion. Lamivudine is well tolerated with few serious adverse events, even in patients with decompensated cirrhosis. Long term therapy in viraemic patients with advanced fibrosis or cirrhosis delays clinical progression. Adefovir dipivoxil is an oral prodrug of adefovir. 10 mg daily is effective in suppressing both wild-type HBV and YMDD mutants, normalising ALT and improving histology. Adefovir dipivoxil has been shown to be well tolerated in longterm therapy. Renal toxicity reported in higher dosages is rarely seen except among patients with creatinine clearance less than 50 ml/min. Adefovir resistance may emerge and the overall rate is much lower than lamivudine, reaching 18% after 4 years of therapy. Adefovir-resistant mutants (rt N236T) are susceptible to lamivudine and entecavir. Little data is available for durability of response off therapy. Entecavir is an oral nucleoside analogue with a recommended dosage of 0.5 mg daily for nucleoside-naive patients, and 1 mg daily for lamivudine-refractory patients. It is a potent antiviral and may also reduced intrahepatitic cccDNA. Entecavir resistance so far has only been detected in lamivudine resistant patients in the one-year studies. Patient counseling is very important to decide on the choice among available therapeutic options. The assessment of the risks/benefits of each option should be carefully explained to individual patient.
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PMID:Chronic hepatitis B--treatment with nucleoside analogues. 1610 69

In the Asia Pacific region Human Immunodeficiency virus (HIV) is often acquired in individuals already infected with hepatitis B virus (HBV). The immune suppression caused by HIV infection reduces cellular immune response against HBV and liver inflammation may improve, but the risk of developing cirrhosis is not. HBV infection does not affect the progression of HIV disease. Anti-retroviral agents may be directly hepatotoxic and cause ALT elevations in patients with chronic hepatitis. Highly active anti-retroviral therapy (HAART) improves immunity and as cytotoxic lymphocyte responses improve, hepatitis flares can occur, usually r within 3 months of initiation of HAART. These hepatitis flares may be followed by normalization of ALT and clearance of HBVDNA. If lamivudine is included in the HAART regime, hepatitis flares may not occur till late and these late flares signal the development of lamivudine resistant HBV strains (90% of HBV/HIV co-infection). Treatment options for chronic HBV infection include interferon (IFN), and nucleoside analogues. Lamivudine, adefovir dipivoxil, tenofovir disoproxil fumarate (DF) are nucleoside analogues with activity against both HBVDNA polymerase and HIV reverse transcriptase. The latter two compounds have added activity against lamivudine resistant HBVDNA. Lamivudine should be avoided in the initial treatment of both hepatitis B as well as HIV because of the high incidence of resistance. Interferon should be considered first for treatment of HBV in HIV co-infected individuals and is usually unsuccessful in the later stages of HIV infection when immune suppression is extreme. As new and improved agents in HAART continue to prolong survival, the use of liver transplantation for cirrhotic patients co-infected with HIV and HBV may increase.
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PMID:Treatment of chronic hepatitis B in HIV co-infected patients. 1610 74

Hepatitis B virus (HBV) is a serious cause of morbidity and mortality in hepatitis B surface (HBsAg) antigen-positive patients treated with chemotherapy. Because the hepatitis is related to HBV virological reactivation, application of effective antiviral therapy, such as Lamivudine, has been attempted. Despite the use of these antiviral agents at the time of clinical hepatitis, some HBsAg-positive patients still develop hepatic failure and die. We used the Molecular Adsorbent Recirculating System (MARS) (MARS Monitor; Teraklin AG, Rostock, Germany) to treat 5 HBsAg-positive lymphoma patients with acute hepatic failure due to chemotherapy despite lamivudine treatment. Before and after each treatment we monitored the parameters of neurological status (EEG, cerebral CT and Glasgow coma score), hemodynamic parameters, acid-base equilibrium and blood gases as well as hepatic and renal function. The inclusion criteria were these of the King's College Hospital. Statistical analysis by Student t method showed significant results (P < .01). Three of 5 patients are alive without signs of reactivation of viral or hematological diseases at 1 year follow-up. The 2 patients died because MARS treatment was started too late, with Glascow coma score grade IV, hemodynamic instability, and mechanical ventilator assistance. Despite the limited number of cases, we believe that MARS can be applied to patients with a high tolerance and yield good results, but the treatment has to start at the first signs of hepatic failure.
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PMID:Molecular adsorbent recirculating system treatment for acute hepatic failure in patients with hepatitis B undergoing chemotherapy for non-Hodgkin's lymphoma. 1618 43

Lamivudine has demonstrated efficacy in the treatment and prevention of hepatitis B virus (HBV) reactivation after hematopoietic stem cell transplantation (HSCT). However, most of these studies involved short durations of prophylaxis, so there is significant concern regarding lamivudine resistance in these patients. Between March 1984 and November 2002, 71 HBV surface antigen-positive HSCT recipients, including a subgroup of 16 who received pretransplantation lamivudine therapy, which was continued into the posttransplantation period to prevent reactivation hepatitis, were enrolled onto our study. The efficacy of lamivudine therapy was first evaluated for the subgroup of 16 patients in terms of treatment response, lamivudine resistance, and viral recurrence after discontinuation by using virologic assays. Efficacy was then evaluated for all patients in terms of the hazards of lamivudine therapy for reactivation hepatitis after transplantation. During a median lamivudine therapy period of 73 weeks (range, 19-153 weeks), the initial response showed a median reduction of 2.54 log10 in serum HBV DNA (-0.28 to 6.72 range). Lamivudine-resistant mutations were detected in 10 (63%) of 16 patients during therapy, and 1 (12%) of 16 patients finally developed a viral breakthrough. At a median follow-up of 30 months after discontinuation, 3 (27%) of 11 cases had recurrence of HBV infection. Despite the emergence of the mutations, no deaths were due to HBV reactivation or severe cases of hepatitis. In the Cox proportion regression model regarding reactivation hepatitis after transplantation of all enrolled patients, lamivudine therapy was found to be the only favorable factor for the event, with a hazard ratio of 0.122 (95% confidence interval, 0.016-0.908; P = .040). In conclusion, extended lamivudine therapy is safe and effective for the prevention of HBV reactivation in an HSCT setting and significantly decreases reactivation hepatitis after transplantation.
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PMID:Extended lamivudine therapy against hepatitis B virus infection in hematopoietic stem cell transplant recipients. 1639 72

We present a case of chronic hepatitis B with membranous nephropathy, that was improved by lamivudine treatment. A 37-year-old man was admitted to our hospital for the evaluation of proteinuria. He was diagnosed as having chronic glomerulonephritis associated with chronic hepatitis B. Histopathological findings of the renal biopsy specimen indicated membranous nephropathy. He suffered from nephrotic syndrome associated with leg edema, which was parallel to the exacerbation of hepatitis. Lamivudine was started for the treatment of hepatitis, which caused the disappearance of serum hepatitis B virus DNA and the normalization of ALT level in 4 weeks. Additionally, proteinuria disappeared 120 weeks after the treatment was started. Lamivudine treatment may remit HBV-associated nephropathy.
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PMID:Successful treatment of hepatitis B virus-associated membranous nephropathy with lamivudine. 1642 43

Up to now Interferon (IFN) has been the only licensed treatment for chronic type B and D viral hepatitis. However, IFN monotherapy is efficacious only in HBeAg positive chronic hepatitis B and is aggravated by important side effects in many patients. To overcome the limits of IFN monotherapy, combination therapies of this cytokine together with other synergistic drugs have been proposed and many antivirals that directly act on Hepatitis B Virus (HBV) synthesis have been developed. Combination therapies with acyclovir, levamisole, and cortisone have not been more advantageous than IFN alone. Of the antivirals, Adenine Arabinoside monophosphate, though active against HBV, causes severe neurotoxicity and Famciclovir has not shown significant efficacy in a large multicenter study of chronic HBeAg positive hepatitis. Lamivudine appears the most promising in terms of clinical benefit, safety and tolerance. It is active on wild type HBV as well as on HBeAg-minus variants of the virus. However, although HBV is consistently repressed while on therapy, only a part of the patients are cured or remain in remission after Lamivudine withdrawal. Maintenance therapy is in order, but the long-term use of Lamivudine is complicated by the emergence of polymerase gene-mutants which may recapitulate disease. Combination with other antivirals active also against Lamivudine escape mutants opens promising new prospects. There is as yet no valid therapy for chronic HDV hepatitis; IFN is of no benefit in most cases.
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PMID:Therapy for chronic hepatitis B. Present status. 1649 43

Hepatitis B virus reactivation-related hepatitis is a serious cause of liver-related morbidity and mortality in inactive hepatitis B virus carriers with hemato/oncological malignancies who receive chemo/immunosuppressive therapy. It occurs in 14% to 50% of such individuals and the mortality ranges from 3.7% to 60%. The aims of the present review were 1) to determine the effect of lamivudine prophylaxis in inactive hepatitis B virus carriers with hemato/oncological malignancies who receive chemo/immunosuppressive therapy, and 2) to define the safety and duration of lamivudine in such individuals. The data currently available suggest that all individuals with hemato/oncological malignancies who undergo chemo/immunosuppressive therapy should be screened for hepatotropic viruses. Lamivudine prophylaxis in inactive hepatitis B virus carriers with hemato/oncological malignancies who receive chemo/immunosuppressive therapy prevents chemo/immunosuppressive-induced hepatitis B virus reactivation. Lamivudine also prevents interruptions in treatment as a result of hepatitis B virus reactivation. Lamivudine is safe and tolerable in such individuals. The ideal protocol of lamivudine prophylaxis for the prevention of hepatitis B virus reactivation in such individuals is not yet established. However, it would appear prudent to begin lamivudine at the time of the initiation of the chemo/immunosuppressive therapy and to continue it throughout the period of chemo/immunosuppressive administration and for at least one but possibly two years following the therapy discontinuation.
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PMID:Anti-viral prophylaxis in inactive hepatitis B virus carriers with hemato-oncological malignancies who receive chemotherapy. 1655 5

Pancytopenia is rare after acute hepatitis B infection. The use of lamivudine in the treatment of acute hepatitis B-associated pancytopenia in renal transplant recipients has not been documented. Herein we reported a 21-year-old woman who was infected with acute hepatitis B 6 months after renal transplantation, a condition complicated by pancytopenia. Lamivudine reversed the acute hepatitis in 1 month and the pancytopenia after 3 months, without a change in renal function. Lamivudine was maintained for 2 years without a hepatitis flare-up after 4 years.
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PMID:Lamivudine reverses severe acute hepatitis B and pancytopenia after renal transplantation: a case report. 1711 16

Hepatitis B immunoglobulin (HBIg) and lamivudine combination has been accepted as the best way to control hepatitis B recurrence after liver transplantation. However, the optimal dose of HBIg and the target titer of hepatitis B surface antibody (HBsAb) remain unclear. We report our satisfactory experience with high-dose HBIg in the early period followed by low-dose HBIg with lamivudine. Subjects comprised five patients with fulminant hepatitis (FH) and 18 patients with liver cirrhosis (LC) who underwent liver transplantation. HBIg at a dosage of 200 IU/kg per day was administered for one week postoperatively. Thereafter, HBIg was administered only for HBsAb titer <100 IU/L. After six months, HBIg was withdrawn in FH and administered in LC only for HBsAb titer <10 IU/L. Lamivudine was administered to two FH and all LC cases. Although two patients with LC showed transient hepatitis B surface antigen (HBsAg) recurrence, all patients remained HBsAg-negative at the final follow-up date. This method allows reliable and cost-effective control of hepatitis B recurrence.
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PMID:Short-term high-dose followed by long-term low-dose hepatitis B immunoglobulin and lamivudine therapy prevented recurrent hepatitis B after liver transplantation. 1726 22

Hepatitis B virus (HBV) has been classified into eight genotypes and can be further divided into several subgenotypes that have different geographic distributions. Because of increased human migration, the prevalence of rare subgenotypes is increasing in Japanese patients with acute hepatitis B. Lamivudine-resistant strains of HBV have begun to emerge in association with chronic hepatitis B. The aim of this study was to investigate the distribution of HBV subgenotypes and lamivudine-resistant strains in patients in Japan with acute hepatitis B. One hundred twenty-three patients with acute hepatitis B and 123 with chronic hepatitis B were studied. HBV subgenotypes and lamivudine-resistance mutations were determined by direct sequencing of the preS and polymerase region, respectively. HBV subgenotypes Aa (n=3), Ae (n=23), Ba (n=7), Bj (n=3), Cs (n=7), Ce (n=76), D (n=2), and H (n=2) were detected in patients with acute hepatitis. In patients with chronic hepatitis, HBV subgenotypes Ae (n=4), Ba (n=1), Bj (n=18), and Ce (n=100) were found. Non-common Japanese subgenotypes, that is, non-Bj and non-Ce, were detected more frequently in patients with acute hepatitis (35.8%) than in patients with chronic hepatitis (4.1%) (Odds ratio, 0.076; 95%CI, 0.029-0.200; P<0.0001). Lamivudine-resistance mutations were detected in chronic hepatitis patients with breakthrough hepatitis but not in other patients. In conclusion, the prevalence of uncommon Japanese HBV subgenotypes is expected to increase, although lamivudine-resistant strains have not yet been found in patients with acute hepatitis B.
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PMID:Comparison of hepatitis B virus subgenotypes in patients with acute and chronic hepatitis B and absence of lamivudine-resistant strains in acute hepatitis B in Japan. 1731 32


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